scholarly journals Kaempferol Blocks the Skin Fibroblastic Interleukin 1β Expression and Cytotoxicity Induced by 12-O-tetradecanoylphorbol-13-acetate by Suppressing c-jun N-terminal Kinase

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3079
Author(s):  
Su-Ji Park ◽  
Do-Wan Kim ◽  
Seong-Ryeong Lim ◽  
Junghee Sung ◽  
Tae Hoon Kim ◽  
...  
Keyword(s):  
Fruits And Vegetables ◽  
Nuclear Factor Kappa B ◽  
Caspase 3 ◽  
Dermal Fibroblasts ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
Normal Human ◽  
Normal Human Dermal Fibroblasts ◽  
Pro Inflammatory Cytokines

Kaempferol, a bioflavonoid present in fruits and vegetables, has a variety of antioxidant and anti-inflammatory capacities, but the functional role of kaempferol in oxidative skin dermal damage has yet to be well studied. In this study, we examine the role of kaempferol during the inflammation and cell death caused by 12-O-tetradecanoylphorbol-13-acetate (TPA) in normal human dermal fibroblasts (NHDF). TPA (5 μM) significantly induced cytotoxicity of NHDF, where a robust increase in the interleukin (IL)-1β mRNA among the various pro-inflammatory cytokines. The skin fibroblastic cytotoxicity and IL-1β expression induced by TPA were significantly ameliorated by a treatment with 100 nM of kaempferol. Kaempferol blocked the production of the intracellular reactive oxygen species (ROS) responsible for the phosphorylation of c-jun N-terminal kinase (JNK) induced by TPA. Interestingly, we found that kaempferol inhibited the phosphorylation of nuclear factor-kappa B (NF-κB) and the inhibitor NF-κB (IκBα), which are necessary for the expression of cleaved caspase-3 and the IL-1β secretion in TPA-treated NHDF. These results suggest that kaempferol is a functional agent that blocks the signaling cascade of the skin fibroblastic inflammatory response and cytotoxicity triggered by TPA.

scholarly journals Anti-Inflammatory Effect of ETAS®50 by Inhibiting Nuclear Factor-κB p65 Nuclear Import in Ultraviolet-B-Irradiated Normal Human Dermal Fibroblasts

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Ken Shirato ◽  
Tomoko Koda ◽  
Jun Takanari ◽  
Takuya Sakurai ◽  
Junetsu Ogasawara ◽  
...  
Keyword(s):  
Uv Irradiation ◽  
Nuclear Import ◽  
Dermal Fibroblasts ◽  
Nuclear Factor ◽  
Human Dermal Fibroblasts ◽  
Protein Levels ◽  
Proinflammatory Responses ◽  
Normal Human ◽  
Anti Inflammatory ◽  
Normal Human Dermal Fibroblasts

Ultraviolet (UV) irradiation induces proinflammatory responses in skin cells, including dermal fibroblasts, accelerating premature skin aging (photoaging). ETAS 50, a standardized extract from theAsparagus officinalisstem, is a novel and unique functional food that suppresses proinflammatory responses of hydrogen peroxide-stimulated skin fibroblasts and interleukin- (IL-) 1β-stimulated hepatocytes. To elucidate its antiphotoaging potencies, we examined whether ETAS 50 treatment after UV-B irradiation attenuates proinflammatory responses of normal human dermal fibroblasts (NHDFs). UV-B-irradiated NHDFs showed reduced levels of the cytosolic inhibitor of nuclear factor-κBα(IκBα) protein and increased levels of nuclear p65 protein. The nuclear factor-κB nuclear translocation inhibitor JSH-23 abolished UV-B irradiation-induced IL-1βmRNA expression, indicating that p65 regulates transcriptional induction. ETAS 50 also markedly suppressed UV-B irradiation-induced increases in IL-1βmRNA levels. Immunofluorescence analysis revealed that ETAS 50 retained p65 in the cytosol after UV-B irradiation. Western blotting also showed that ETAS 50 suppressed the UV-B irradiation-induced increases in nuclear p65 protein. Moreover, ETAS 50 clearly suppressed UV-B irradiation-induced distribution of importin-αprotein levels in the nucleus without recovering cytosolic IκBαprotein levels. These results suggest that ETAS 50 exerts anti-inflammatory effects on UV-B-irradiated NHDFs by suppressing the nuclear import machinery of p65. Therefore, ETAS 50 may prevent photoaging by suppressing UV irradiation-induced proinflammatory responses of dermal fibroblasts.

3-methyladenine inhibits procollagen-1 and fibronectin expression in dermal fibroblasts independent of autophagy

2020 ◽  
Vol 20 ◽  
Author(s):  
Ji-yong Jung ◽  
Hyunjung Choi ◽  
Eui-Dong Son ◽  
Hyoung-june Kim
Keyword(s):  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Pi3k Inhibitors ◽  
Ecm Proteins ◽  
Autophagy Inhibitor ◽  
Normal Human ◽  
Phosphoinositide 3 Kinase ◽  
Interfering Rna ◽  
Normal Human Dermal Fibroblasts

Background: Autophagy is deeply associated with aging, but little is known about its association with the extracellular matrix (ECM). 3-methyladenine (3-MA) is a commonly used autophagy inhibitor. Objective: We used this compound to investigate the role of autophagy in dermal ECM protein synthesis. Method: Normal human dermal fibroblasts (NHDFs) were treated with 3-MA for 24 h, and mRNA encoding several ECM proteins was analyzed in addition to the protein expression of procollagen-1 and fibronectin. Several phosphoinositide 3-kinase (PI3K) inhibitors, an additional autophagy inhibitor, and small interfering RNA (siRNA) targeting autophagy-related genes were additionally used to confirm the role of autophagy in ECM synthesis. Method: Normal human dermal fibroblasts (NHDFs) were treated with 3-MA for 24 h, and mRNA encoding several ECM proteins was analyzed in addition to the protein expression of procollagen-1 and fibronectin. Several phosphoinositide 3-kinase (PI3K) inhibitors, an additional autophagy inhibitor, and small interfering RNA (siRNA) targeting autophagy-related genes were additionally used to confirm the role of autophagy in ECM synthesis. Results: Only 3-MA, but not other chemical compounds or autophagy-related gene-targeting siRNA, inhibited the transcription of procollagen-1- and fibronectin-encoding genes. Further, 3-MA did not affect the activation of regulatory Smads, but inhibited the interaction between Smad3 with p300. Moreover, 3-MA treatment increased the phosphorylation of cAMP response element-binding protein (CREB); however, CREB knock-down did not recover 3-MA-induced procollagen-1 and fibronectin downregulation. Conclusion: We revealed that 3-MA might inhibit procollagen-1 and fibronectin synthesis in an autophagy-independent manner by interfering with the binding between Smad3 and p300. Therefore, 3-MA could be a candidate for the treatment of diseases associated with the accumulation of ECM proteins.

scholarly journals The role of nuclear factor kappa B in human labour

Reproduction ◽  
2005 ◽  
Vol 130 (5) ◽  
pp. 569-581 ◽  
Author(s):  
Tamsin M Lindström ◽  
Phillip R Bennett
Keyword(s):  
Nuclear Factor Kappa B ◽  
Inflammatory Cells ◽  
Nuclear Factor ◽  
Mortality And Morbidity ◽  
Nuclear Factor Kappa ◽  
Human Labour ◽  
Term Labour ◽  
Labour Onset ◽  
Pro Inflammatory Cytokines

Preterm birth remains the leading cause of perinatal mortality and morbidity, largely as a result of a poor understanding of the precise mechanisms controlling labour onset in humans. Inflammation has long been recognised as a key feature of both preterm and term labour, with an influx of inflammatory cells into the uterus and elevated levels of pro-inflammatory cytokines observed during parturition. Nuclear factor kappa B (NF-κB) is a transcription factor family classically associated with inflammation. Accumulating evidence points to a role for NF-κB in the physiology and pathophysiology of labour. NF-κB activity increases with labour onset and is central to multiple prolabour pathways. Premature or aberrant activation of NF-κB may thus contribute to preterm labour. The current understanding of NF-κB in the context of human labour is discussed here.

scholarly journals IGF-1 Upregulates Biglycan and Decorin by Increasing Translation and Reducing ADAMTS5 Expression

2021 ◽  
Vol 22 (3) ◽  
pp. 1403
Author(s):  
Hanon Lee ◽  
Jiyeong Lim ◽  
Jang-Hee Oh ◽  
Soyun Cho ◽  
Jin Ho Chung
Keyword(s):  
Protein Expression ◽  
Actinomycin D ◽  
Protein Translation ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Protein Levels ◽  
Mrna And Protein Expression ◽  
Normal Human ◽  
Normal Human Dermal Fibroblasts

Proteoglycan (PG) is a glycosaminoglycan (GAG)-conjugated protein essential for maintaining tissue strength and elasticity. The most abundant skin PGs, biglycan and decorin, have been reported to decrease as skin ages. Insulin-like growth factor-1 (IGF-1) is important in various physiological functions such as cell survival, growth, and apoptosis. It is well known that the serum level of IGF-1 decreases with age. Therefore, we investigated whether and how IGF-1 affects biglycan and decorin. When primary cultured normal human dermal fibroblasts (NHDFs) were treated with IGF-1, protein levels of biglycan and decorin increased, despite no difference in mRNA expression. This increase was not inhibited by transcription blockade using actinomycin D, suggesting that it is mediated by IGF-1-induced enhanced translation. Additionally, both mRNA and protein expression of ADAMTS5, a PG-degrading enzyme, were decreased in IGF-1-treated NHDFs. Knockdown of ADAMTS5 via RNA interference increased protein expression of biglycan and decorin. Moreover, mRNA and protein expression of ADAMTS5 increased in aged human skin tissues compared to young tissue. Overall, IGF-1 increases biglycan and decorin, which is achieved by improving protein translation to increase synthesis and preventing ADAMTS5-mediated degradation. This suggests a new role of IGF-1 as a regulator for biglycan and decorin in skin aging process.

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